POS1079 COMPARISON OF CHOLESTEROL PROFILE CHANGES AFTER TREATMENT WITH BIOLOGICS OR JANUS KINASE INHIBITORS IN PATIENTS WITH RHEUMATOID ARTHRITIS
Authors: J. H. Koh, B. W. Lee, W. U. Kim
Journal: Annals of the Rheumatic Diseases (2023)

<h3>Background</h3> Janus kinase inhibitor (JAKi) and tumor necrosis factor inhibitor (TNFi) both effectively reduce inflammation, and both increases serum lipid levels. However, in the recent phase 3b-4 trial, major adverse cardiovascular events were higher with tofacitinib than TNFi. Cholesterol is still primary to the development of atherosclerosis, which collaborates with inflammation. Even in the young population, mildly abnormal lipid levels were associated with an increased future risk of atherosclerotic cardiovascular disease events. <h3>Objectives</h3> To assess the effects of biological and targeted synthetic disease-modifying anti-rheumatic drugs (DMARDs) on lipid profiles in patients with moderate-to-severe rheumatoid arthritis (RA). <h3>Methods</h3> This retrospective single-center observational study included patients with RA who initiated and maintained tumor necrosis factor-α inhibitor (TNFi), abatacept, tocilizumab, and Janus kinase inhibitor (JAKi) for at least 6 months. Changes in lipid profile were assessed at months 3 and 6, and associations with clinical efficacy, concomitant medications, and co-morbidities were evaluated. <h3>Results</h3> This study included 114 patients treated with TNFi, 81 patients with abatacept, 103 patients with tocilizumab, and 89 patients with JAKi. Median percent change from baseline to 6 months in total cholesterol, low-density lipoprotein-cholesterol (LDL-C), high-density lipoprotein cholesterol (HDL-C), and non-HDL-C levels were higher in tocilizumab and JAKi versus TNFi and abatacept recipients (16% and 15% vs 6% and 3%, 19% and 24% vs 8% and 3%, 5% and 9% vs 3% and 0%, 19% and 19% vs 7% and 8%, respectively). The significant change in non-HDL-C was associated with JAKi (versus TNFi, OR, 2.671; 95% CI, 1.44–4.956), tocilizumab (versus TNFi, OR, 1.996; 95% CI, 1.087–3.665), concomitant glucocorticoids (OR, 2.802, 95% CI 1.344–5.843), and statin (OR, 0.419; 95% CI 0.230–0.765), and presence of rheumatoid factor (OR, 3.252, 95% CI, 1.029–10.276). However, the change in disease activity in 28 joints was not associated with a significant non-HDL-C change. <h3>Conclusion</h3> Regardless of disease activity changes, tocilizumab and JAKi-associated increases in serum non-HDL-C levels were observed. Combination with glucocorticoids may induce elevations in non-HDL-C, whereas statins may decrease in non-HDL-C. <h3>References</h3> [1] Nurmohamed MT, Heslinga M, Kitas GD. Cardiovascular comorbidity in rheumatic diseases. <i>Nat Rev Rheumatol</i> 2015;11:693-704. [2] Robertson J, Peters MJ, McInnes IB<i>, et al.</i> Changes in lipid levels with inflammation and therapy in RA: a maturing paradigm. <i>Nat Rev Rheumatol</i> 2013;9:513-23. [3] Brunner FJ, Waldeyer C, Ojeda F<i>, et al.</i> Application of non-HDL cholesterol for population-based cardiovascular risk stratification: results from the Multinational Cardiovascular Risk Consortium. <i>Lancet</i> 2019;394:2173-83. <h3>Acknowledgements</h3> This work was supported by National Research Foundation of Korea grants funded by the Ministry of Science, ICT and Future Planning (Grant 2015R1A3A2032927 to W.U. Kim). <h3>Disclosure of Interests</h3> None Declared.